Normobaric oxygen for cerebral ischemic injury.

Normobaric oxygen for cerebral ischemic injury.
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常压氧治疗脑缺血损伤

DOI:
10.3969/j.issn.1673-5374.2013.31.001
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发表时间:
2013-11-05
影响因子:
6.1
通讯作者:
Zhou C
Zhou C
中科院分区:
医学2区
文献类型:
--
作者:
Chen C;Cui H;Li Z;Wang R;Zhou C

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吸氧可增加脑缺血/再灌注损伤后组织的氧气供应,保护受损的神经细胞。然而,高压氧可能会加剧氧化应激。相比之下,常压氧具有快速、无创的特点,可能对缺血性/缺氧性疾病具有治疗作用。大鼠吸入常压氧气(95%O2),连续6d,建立大鼠局灶性脑缺血模型。Nissl和2,3,5-三苯基四氮唑(TTC)染色显示,常压氧预处理可改善神经功能缺失,缩小脑梗塞体积。免疫组织化学染色和Western印迹分析显示缺氧诱导因子-1α、Notch-1、血管内皮生长因子和促红细胞生成素的表达增加。行为研究也证实了神经缺陷分数的增加。缺氧诱导因子抑制剂2-甲氧基雌二醇在常压氧前1h处理可抑制常压氧的保护作用。鉴于这些观察,常压氧预处理可能通过低氧诱导因子信号通路减轻脑缺血损伤。
Oxygen inhalation has been shown to increase oxygen supply to tissues after cerebral ischemia/ reperfusion injury, protecting injured neural cells. However, hyperbaric oxygen may aggravate oxidative stress. By contrast, normobaric oxygen has the rapid and non-invasive characteristics and may have therapeutic effects on ischemic/hypoxic disease. Rats inhaled normobaric oxygen (95% O2) for 6 consecutive days, and then a rat model of focal cerebral ischemia was established. Nissl and 2,3,5-triphenyltetrazolium chloride (TTC) staining revealed that normobaric oxygen pretreatment improved neurological deficits and reduced infarct volume. Immunohistochemical staining and western blot assay revealed that the expression of hypoxia-inducible factor-1α, Notch-1, vascular endothelial growth factor and erythropoietin were increased. Behavioral studies also verified that neurological deficit scores increased. The hypoxia-inducible factor inhibitor 2-methoxyestradiol treatment at 1 hour before administration of normobaric oxygen could suppress the protective effect of normobaric oxygen. Given these observations, normobaric oxygen pretreatment may alleviate cerebral ischemic injury via the hypoxia-inducible factor signal pathway.
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